The Ebola virus comes from the Filoviridae family, similar to the Marburg virus. It is named after the Ebola River in Zaire, Africa, near where the first outbreak was noted by Dr. Ngoy Mushola in 1976 after a significant outbreaks in both Yambuku, Zaire (now the Democratic Republic of the Congo), and Nzara, in western Sudan. There are three distinct species of Ebola virus which cause fatal disease in humans: Zaire ebolavirus (ZEBOV) (also known as EBOV), Sudan ebolavirus (SEBOV) and Ivory Coast ebolavirus (ICEBOV).
Among humans, the Ebola virus is transmitted by direct contact with infected body fluids such as blood. The incubation period of Ebola virus infection varies from two days to four weeks. Symptoms are variable too, but the onset is usually sudden and characterised by high fever, prostration, myalgia, arthralgia, abdominal pains and headache. These symptoms progress to vomiting, diarrhea, oropharyngeal lesions, conjunctivitis, organ damage (notably the kidney and liver) by co-localized necrosis, proteinuria, and bleeding both internal and external, commonly through the gastrointestinal tract. Death or recovery to convalescence occurs within six to ten days of onset of symptomology.
Although several antivirals have shown efficacy against Ebola virus infection in vitro or in animal models, none of them have been yet assessed in human beings with Ebola virus disease. Thus, there exists a hurge need in the art for an effective curative treatment against Ebola Virus Disease. Potential drug candidates include Favipiravir a nucleotide analogue approved for novel or re-emerging influenza in Japan (Furuta et al., 2013).
Indeed, results of two independent studies in mice infected with Ebola virus recently showed that the initiation of 150 mg/kg Favipiravir twice a day within 6 days of infection induced rapid virus clearance, reduced biochemical parameters of disease severity, and led to 100% survival (Smither et al., 2014 and Oestereich et al., 2014).